Abstract
Background: We have demonstrated that Kupffer cell-derived cytokines are the major cause of parenchymal liver injury during acute pancreatitis and that inhibition of protein kinase C-zeta (PKC-zeta) within Kupffer cells downregulates cytokine production and attenuates pancreatitis-induced liver injury. Since Toll-like receptor-4 (TLR4) plays a critical role in macrophage activation during sepsis, we tested the hypothesis that TLR4 activates PKC-zeta and that deletion of TLR4 attenuates liver injury in experimental pancreatitis.
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